A recent study1 of rat vascular smooth muscle cells (VSMCs) in culture reports strong protective effects by selenium (in the form of sodium selenite) against calcification, frequently associated with atherosclerosis. Vascular calcification has been associated with oxidative stress, such as that of hydrogen peroxide, minimally modified oxidized LDL and different lipid peroxidation products.

Vascular calcification is an amazing (though damaging) process. VSMCs actually become induced (by oxidative stress, for example) to undergo differentiation to function like osteoblasts (bone-making cells). This osteoblastic differentiation is characterized by the expression of multiple bone-related molecules including ALP, Col I, and OC [osteocalcin] and upregulation of Runx2, a key transcription factor during osteoblastic differentiation of VSMCs.1 The researchers explained that a growing body of evidence pointed to the importance of the activation of the ERK (extracellular signal- regulated kinase) pathway in the osteoblastic differentiation of VSMCs. They found that “sodium selenite alone at 0.1μM did not affect the level of ERK phosphorylation [activation](data not shown), but markedly inhibited H2O2 [hydrogen peroxide]-induced ERK activation [in the VSMCs].”

Moreover, the researchers showed that the intracellular ROS (reactive oxygen species) generation and MDA (malondialdehyde, a major lipid peroxidation product) content were significantly increased in the hydrogen peroxide treated VSMCs, while the content of protein thiols (that include molecules such as glutathione) and glutathione peroxidase activity were significantly decreased (indicating oxidative stress) after hydrogen peroxide treatment. Pretreatment with 0.1 μM sodium selenite for 24 hours significantly reversed the effects of hydrogen peroxide on intracellular ROS generation and the cellular contents of MDA and protein thiols.

The authors conclude: “These results indicate a potential preventive role for Se in vascular calcification, suggesting that vascular calcification may be another target of Se action in anti-atherosclerosis. However, our conclusion is just drawn from in vitro experiment. Due to the potential side effects of Se, the safety [of] using Se as [a] preventive drug for vascular calcification needs to be further addressed in animal experiments, especially in human experiments.”

We both take 400 μg of selenium per day in the form of sodium selenite. This is the upper limit of selenium doses considered safe by the Institute of Medicine of the National Academy of Sciences.